Met 2: Cardio; Lec. 15 A Fib

Front 1

True or false: the onset and offset of SVT are both gradual.

Back 1

False.

Usually sudden onset and offset - this differentiates SVT from sinus tachycardia, which is gradual.

Front 2

List common symptoms of SVT

Back 2

palpitations
heart-racing
chest discomfort
dyspnea

Front 3

Describe the mechanism of reentry in AVNRT.

Back 3

Two pathways - one fast conducting with long RP and one slow conducting with short RP.

Premature beat hits AV node, makes the fast pathway refractory because it has fallen within this pathway's RP. Impulse goes through slow pathway, and if the tissue in the fast pathway has recovered and is no longer refractory, re-entry occurs.

Front 4

What is pre-excitation and how does it manifest on ECG?

Back 4

Activation of ventricles via accessory pathway BEFORE the AV node has conducted its impulse.

Appears on ECG as a delta wave, slurred QRS, and short PR interval.

Front 5

True or false: accessory pathways only conduct impulses in a forward direction towards the ventricles.

Back 5

False.

Most conduct both ways, but there are some that conduct only forwards or only retrograde.

You need to have forward conduction for pre-excitation to occur.

Front 6

What is Wolfe Parkinson White syndrome?

Back 6

A syndrome in which there is evidence of pre-excitation via accessory pathway and symptoms of tachyarrhythmia.

Front 7

How does reentry occur in orthodromic AVRT? What does the QRS complex look like on ECG?

Back 7

Impulse does not conduct through the accessory pathway because it is refractory.

Impulse conducts forward through the AV node, to the ventricles, and back up to the atria through the accessory pathway leading to re-entry.

Narrow QRS complex

Front 8

What is the big difference between AVRT/AVNRT and atrial tachycardia?

Back 8

Atrial tachycardia does NOT require the AV node or the ventricles and therefore does not need a QRS associated with every P wave.

AVRT and AVNRT both require atrium, AV node, ventricles all to be functioning.

Front 9

What is the most common cause of atrial tachycardia?

Back 9

Usually caused by enhanced automaticity at a focal area in the atrium - idiopathic etiology

Front 10

What is the initial treatment of choice in unstable SVT?

Back 10

Synchronized DC cardioversion

Front 11

What maneuvers can aid in terminating AVRNT or AVRT in a patient?

Back 11

Valsalva and vagal manuevers affect AV nodal conduction and abruptly terminate these arrhythmias

Front 12

What can result from tachycardia induced cardiomyopathy?

Back 12

Heart failure and death

Front 13

What are ECG characteristics in atrial fibrillation?

Back 13

Chaotic atrial activity with an irregularly irregular response

Front 14

Atrial fibrillation can be characterized into three main patterns - what are they?

Back 14

Paroxysmal - self terminating episodes <1 wk
Persistent - longer than one week, may not terminate without cardioversion
permanent - present for more than one year. Refractory to cardioversion

Front 15

What is an example of a vagal maneuver?

Back 15

Carotid sinus massage

Front 16

A patient with SVT performs a Valsalva maneuver ("bears down") in an attempt to terminate the arrhythmia, but they are unsuccessful and the arrhythmia continues. What does this tell you? What type of SVT might this be?

Back 16

The AV node is not in the circuit as the Valsalva would have stopped it.

This indicates the SVT is atrial tachycardia.

Front 17

A patient tells you they experience their SVT symptoms every day. What can you use to document the tachycardia?

Back 17

Holter monitor - 24-48h continuous recording

If the symptoms were less often, can use event recorders (loop or non looping)

Front 18

What is a potential outcome in a patient with both WPW/pre-excitation AND atrial fibrillation? What is the treatment of choice for these patients?

Back 18

Ventricular fibrillation - this is the mechanism of SCD in these patients.

Treatment of choice is catheter ablation

Front 19

What is the characteristic rhythm on ECG of atrial fibrillation?

Back 19

Irregularly irregular

Front 20

What is a common trigger for atrial fibrillation?

Back 20

Rapid activity from the pulmonary veins

some AFib is related to structural heart disease: CHF, mitral valve disesase, HTN, LVH

Front 21

What are some electrophysiological abnormalities that can predispose a person to atrial fibrillation?

Back 21

Fibrosis and remodeling (eg. from previous MI, previous AFib leading to dilation and fibrosis)
Cardiac ion channelopathies
Atrial ectopic triggers (eg. pulmonary veins)

Front 22

True or false: atrial fibrillation can be present for more than a year.

Back 22

True.

This is 'permanent atrial fibrillation' refractory to cardioversion.

Front 23

What are the three main goals of treatment in atrial fibrillation?

Back 23

1) Prevent thromboembolism
2) Symptom control
3) Prevention of tachycardia induced cardiomyopathy

Front 24

Why are patients with atrial fibrillation predisposed to increased risk of thromboembolism?

Back 24

The atria are not contracting properly and blood can pool and clot, most commonly in LA appendage

Front 25

What groups of patients with atrial fibrillation are at higher risk for thromboembolism and should be anticoagulated with warfarin/NOA?

Back 25

Valvular heart disease - eg. MV disease
Hypertrophic cardiomyopathy
Increased risk determined by CHADSVASC score

Front 26

What risks are worth 1pt each in the CHADS2 score? When should they be treated with warfarin/NOA?

Back 26

1. CHF
2. HTN
3. Age > 75
4. Diabetes
5. Prior embolization or CVA

CHADS > 1, they get better risk reduction of stroke than without warfarin.

Front 27

What two risks must be balanced in the approach to prevention of thromboembolism in atrial fibrillation?

Back 27

Risk of thromboembolism VS risk of intracranial hemorrhage

Front 28

What is the target INR for warfarin? Why is this the target range?

Back 28

Target INR = 2-3

This provices the lowest risk of stroke AND lowest risk of intracranial bleed

Front 29

True or false: rhythm control is superior to rate control in reducing mortality and risk of stroke.

Back 29

False.

There is no evidence to support one or the other, but rate control is generally first line since it is more simple.

Front 30

When is rhythm control preferred in treatment of atrial fibrillation?

Back 30

- Patients with new or highly symptomatic AF
- Limited by bradycardia

May elect to do DC cardioversion or antiarrhythmic meds with these patients to promote normal rhythm

Front 31

What are the goals for rate control in atrial fibrillation? (resting HR, avg HR, max HR)

Back 31

HR < 80
Avg HR < 100
No HR > 110% of max age predicted

Front 32

What is the mechanism of action of DC cardioversion?

Back 32

Depolarizes all of the heart cells to allow sinus rhythm to come through

Front 33

What is a pro arrhythmia?

Back 33

The generation of a new arrhythmia from antiarrhythmic medication

Front 34

True or false: atrial flutter conveys the same stroke risk as atrial fibrillation.

Back 34

TRUE

Front 35

differential for SVT

Back 35

AT - atrial tachycardia
AVNRT - AV node reentry tachycardia
AVRT - AV reentry tachycardia
AFL - atrial flutter
MAT - multifocal atrial tachycardia

remember that the treatments for VT will work for SVT but the treatments for SVT might kill someone with VT. So when in doubt treat as VT

Front 36

rate control drugs for AFib?

Back 36

bb, verapamil, diltiazem, digoxin

Front 37

considerations for rhythm control?

Back 37

LVEF
age
diuretic use
gender (women are more predisposed to proarrhythmia)

Front 38

rhythm control drugs and their classes

Back 38

flecainide/propafenone - class 1C Na channel blockers, slows conduction)

sotalol (class 3 K channel blocker, prolongs repolarization)

amiodarone (class 3 K channel blocker, BB, inotrope)

Front 39

when do you use which rhythm control agent

Back 39

amiodarone in LV systolic dysfunction

sotalol or amiodarone in CAD with preserved LVEF

don't use sotalol in the elderly women on diuretics (worry about hypoK)

Front 40

T/F rhythm control helps for symptom control and altering stroke risk

Back 40

FALSE

rhythm control only helps for symptoms

Front 41

Why is AFlutter important?

Back 41

carries the same stroke risk as AFib

Front 42

both is AFlutter divided in terms of pahtophys and treatment

Back 42

typical - saw tooth pattern in the inferior leads, rate over 300/min
atypical - everything else

treatment is straightforward for typical Rf ablation (95%) success
atypical flutter more like AFib